FDA has granted orphan drug designation to asedebart (Lu AG13909), Lundbeck's investigational anti-adrenocorticotropic hormone (anti-ACTH) monoclonal antibody, for the treatment of endogenous Cushing syndrome, the company announced September 11, 2026.¹ Endogenous Cushing syndrome is a rare endocrine disorder driven primarily by excess ACTH, which leads to chronic cortisol excess and substantial disease burden. Current treatment options are often limited by suboptimal disease control and treatment-related complications.
Key facts
- Drug: Asedebart (Lu AG13909; Lundbeck)
- Class: Humanized anti-ACTH monoclonal antibody
- Indication: Endogenous (ACTH-dependent) Cushing syndrome
- Regulatory status: FDA orphan drug designation granted September 11, 2026
- Mechanism: Blocks ACTH binding to melanocortin 2 receptor in adrenal glands
- Key trial: BalanCeD (NCT06471829); proof-of-concept, Cushing disease
- Also in development: Proof-of-concept trial in congenital adrenal hyperplasia (CAH)
- Prior designations: EU orphan status (Cushing's, CAH); US orphan status (CAH); Japan orphan status (CAH, Cushing disease)
- Orphan drug benefits: Tax credits, fee exemptions, up to 7 years market exclusivity if approved
- Geography: US designation; global regulatory momentum (EU, Japan)
"The FDA [o]rphan [d]rug [d]esignation is an important step for asedebart and for Lundbeck's growing commitment to rare neuroendocrine disorders," said Tarek Samad, PhD, executive vice president and head of research and development at Lundbeck, in a company press release.¹ "ACTH-dependent Cushing's syndrome can be a devastating condition for patients, with long-term consequences that remain difficult to control despite available treatments. This milestone reflects the strength of the science behind asedebart's development to date and supports our ambition to advance innovative medicines in areas where patients continue to face significant unmet need."
Why is a new treatment needed for ACTH-dependent Cushing syndrome?
ACTH-dependent Cushing syndrome is caused by excess secretion of ACTH, most commonly from a pituitary tumor (Cushing disease) and less often from an ectopic ACTH-secreting tumor. Elevated ACTH drives excess adrenal production of glucocorticoids, mineralocorticoids, and androgens.¹ Sustained cortisol excess contributes to substantial disease burden through metabolic, cardiovascular, and neuropsychiatric complications and is associated with increased morbidity and mortality.¹,²
Achieving and maintaining adequate disease control can be difficult even with existing medical therapies, which vary in efficacy and may be constrained by safety and tolerability considerations.³ Surgery to remove the source of excess ACTH is the preferred first-line treatment when feasible, but not all patients are eligible or achieve sustained remission.¹